Renal Regulation of Acid Base Balance - McCormick Flashcards
What effect does chemical buffers have on pH changes?
Minimize, but can’t prevent changes caused by strong acid or base
Characteristics of volatile acid
Carbonic acid - H2CO3
CO2 - volatile gas
Pulm ventilation controls H2CO3 in body fluids
From oxidative metabolism
Characteristics of fixed acids
Non-carbonic acids - eg. sulfuric, phosphoric
Initially neutralized, ultimately excreted
NOT fixed by ventilation
3 Lines of defense against pH changes
- Chemical buffers - H
- -can be Hb, bone - Respiration - CO2
- Kidneys - HCO3
- -major EC buffer
Why is bicarbonate buffer system so powerful?
Components are abundant
Open system - HCO3 and CO2 readily adjusted by respiration and renal function
Renal response to excess acid
All filtered HCO3 is reabsorbed
Additional H secreted, primarily as NH4
Renal response to excess base
Incomplete reabsorption of filtered HCO3
Decreased H secretion
Secretion of HCO3 in CD
How is most H secreted?
In combination with urinary buffers
- titratable acid - HPO4 most imp
- ammonia
Luminal pH along nephron
GC - 7.4
PT and DT - 6.7
Loop - 7.6
Excreted < 6.0
a-intercalated cells
In CD
Actively secrete acid (H)
H-ATPase
B-intercalated cells
In CD
Actively secrete base (HCO3)
HCO3-Cl exchanger
Acidification in the proximal tubules
Most of the H secreted by PT is used to reabsorb filtered HCO3
-so it only falls slightly to 6.7
If arterial pH is too high, what is kidney response
Respond by incompletely reabsorbing HCO3
Normally 80% reabsorbed in PT, remainder in TAL (saturable)
What is produced from glutamine oxidation
2 NH4
2 HCO3
-way to excrete H
What happens in chronic acidemia (elevated H conc)
Up regulated renal NH4 production and excretion
What happens in alkalemia (reduction in H conc)
B-intercalated cells (CD) secrete HCO3
6 Factors that control renal H secretion
- Decreased intracellular pH
- Increased plasma Pco2
- Carbonic anhydrase activity
- Increased Na reabsorption
- Decreased extracellular K
- Increased plasma aldosterone
What happens from extensive use of diuretics?
ECF contraction - Increased RAAS
Increased tubular secretion of H
Leads to increased reabsorption of all filtered HCO3 and new HCO3
Leads to metabolic alkalosis
What type of acid base disturbance is excessive diuretic use?
Metabolic alkalosis
Respiratory acidosis
Renal response
Increased arterial Pco2
Renal increases H secretion to restore pH
Also increases HCO3
Respiratory alkalosis
Renal response
Decreased arterial Pco2
Renal response leads to less H secretion and more HCO3 excretion
Metabolic acidosis
Low plasma pH
Gain of fixed acid or loss of HCO3
BOTH lead to fall in HCO3
Respiratory compensation to metabolic acidosis
Increased ventilation
Metabolic alkalosis
Abnormally high plasma pH
Excessive gain of strong base or excessive loss of fixed acid (vomit)
Resp compensation - decreased ventilation
If you have pH that is acidotic, what would you expect Pco2 to be if respiratory?
Pco2 > 40 mmHg
Normal range for anion gap?
8-16 mEq/l
Normal or increased depending on cause of metabolic acidosis
Hyperchloremic acidosis
AG unchanged
Loss of HCO3 is matched by gain of Cl-
Normochloremic
High anion gap acidosis
HCO3 is replaced by unmeasured anion
